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K-Cl cotransporters are proteins that lower intracellular chloride concentrations below the electrochemical equilibrium potential. Additionally we are shipping Solute Carrier Family 12 (Potassium-Chloride Transporter) Member 5 Antibodies (116) and Solute Carrier Family 12 (Potassium-Chloride Transporter) Member 5 Kits (1) and many more products for this protein.
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Study describes the developmental patterns of cation-chloride cotransporters in the human brain from the fetal stage to senescence. Expression of KCC2 and its functionally associated proteins begins in early fetal period.
The authors show that APP (show APP Proteins) can physically interact with KCC2, a neuron-specific K(+)-Cl(-) cotransporter (show SLC12A4 Proteins) that is essential for Cl(-) homeostasis and fast GABAergic inhibition.
SLC12A5 promoted the migration and invasion of BUC by enhancing MMP-7 (show MMP7 Proteins) expression.
Study shows that the overall expression of potassium-chloride cotransporter (show SLC12A7 Proteins)-2 is increased in the hippocampi of temporal lobe epilepsy patients.
Our network model suggested the loss of KCC2 in a critical number of pyramidal cells increased external potassium and intracellular chloride concentrations leading to seizure-like field potential oscillations. These oscillations included transient discharges leading to ictal-like field events with frequency spectra as in vitro Restoration of KCC2 function suppressed seizure activity and thus may present a useful therapeut
The KCC2 exerts specific functions for the maturation of glycinergic synapses in cultured spinal cord neurons.
SLC12A5 plays a pivotal oncogenic role in colorectal carcinogenesis; its overexpression is an independent prognostic factor of patients with CRC (show CALR Proteins).
the functional deficit of KCC2 may offer an explanation for the delayed onset of Rett symptoms.
A KCC2 mutation causes epilepsy of infancy with migrating focal seizures. Decreased KCC2 expression, reduced protein glycosylation and impaired Cl- extrusion contribute to loss of KCC2 activity, impairing synaptic inhibition and promoting excitability.
these data provide insight into the mechanism regulating Cl(-) homeostasis in immature neurons, and suggest that WNK1 (show WNK1 Proteins)-regulated changes in KCC2 phosphorylation contribute to the developmental excitatory-to-inhibitory GABA sequence.
This study directly implicates the dephosphorylation and downregulation of KCC2 in the peritumoral brain region in the pathophysiology of tumor-associated epilepsy in disease model mice; proposes that glutamate (show GRIN1 Proteins) release from glioma cells mediate the dephosphorylation and downregulation of KCC2, revealing yet another target for the treatment of tumor-associated epilepsies.
Study showed that there is a transient dysregulation in the levels of NKCC1 (show SLC12A2 Proteins) and KCC2 at disease onset, the time point when heightened nociceptive behaviors are most pronounced in mice with experimental autoimmune encephalomyelitis.
Neonatal maternal separation leads to KCC2 expression inhibition persisting until adolescence in hippocampus.
TGF-beta2 (show TGFB2 Proteins) is a new regulatory factor for KCC2 functional activation and membrane trafficking.
GABAA (show GABRg1 Proteins) receptor (GABAAR (show GABRG2 Proteins)) and the Na(+)-K(+)-2Cl(-) cotransporter (show SLC12A1 Proteins) (NKCC1 (show SLC12A2 Proteins)), but not the K(+)-Cl(-) cotransporter (show SLC12A4 Proteins) (KCC2), were expressed in the terminals of the CRH (show CRH Proteins) neurons at the median eminence (ME). In contrast, CRH (show CRH Proteins) neuronal somata were enriched with KCC2 but not with NKCC1 (show SLC12A2 Proteins).
GluK2 (show GRIK2 Proteins)-mediated increase in KCC2 recycling to the surface membrane translates to a hyperpolarization of the reversal potential for GABA (EGABA).
KCC2 expression supersedes NKCC1 (show SLC12A2 Proteins) in mature fiber cells in mouse and rabbit lenses.
Repeated stress decreased KCC2 expression and increased NKCC1 (show SLC12A2 Proteins) expression in membranes of granular and pyramidal cells in the hippocampus.
Decreasing [Cl(-)]i levels caused by increasing KCC2 levels in the 12 N could play important roles in regulating the frequency of respiration-related rhythmic activity during development.
K-Cl cotransporters are proteins that lower intracellular chloride concentrations below the electrochemical equilibrium potential. The protein encoded by this gene is an integral membrane K-Cl cotransporter that can function in either a net efflux or influx pathway, depending on the chemical concentration gradients of potassium and chloride. The encoded protein can act as a homomultimer, or as a heteromultimer with other K-Cl cotransporters, to maintain chloride homeostasis in neurons. Alternative splicing results in two transcript variants encoding different isoforms.
solute carrier family 12 (potassium/chloride transporter), member 5
, K-Cl cotransporter 2
, electroneutral potassium-chloride cotransporter 2
, furosemide-sensitive K-Cl cotransporter
, neuronal K-Cl cotransporter
, neuronal-specific K-Cl cotransporter
, solute carrier family 12 member 5
, solute carrier family 12, member 5
, erythroid K-Cl cotransporter 2